Monday, November 26, 2007

1.1 Myopia

OK, we all know what myopia is. So what causes it? There is a Nobel Prize in there somewhere if you can come up with the answer. To be specific, we are talking about "school myopia", the type that starts up usually in elementary schools, not those induced by, e.g., cataracts or diabetes mellitus. Of course, there has been a long debate on whether it is nature or nurture. Which is probably irrelevant - if your eyeballs are predisposed to developing myopia, once given the stress, myopization will most likely ensue.

First, let us look at what we do and don't know:

1. Environmental factors: In survey after survey in Asian countries, myopia starts to show in elementary school children, by college years, most students are myopic. In some medical school classes, non-myopes are a rare species. In contrast, in rural areas of China, myopia is not as prevalent as that in the cities in school children of the same age. So now: Too much education (hint: too much reading) is a risk factor? Move medical schools to countryside?

2. Family tradition: If you look into your family photo albums, you'll notice no one wore glasses a few generations back. Not that the glasses were unavailable, mind you. They were. It is definitely in the more recent generations that myopia becomes rampant. A common scenario is a family with one or both grandparents myopic, so are the parents, and chances are the next generation will also be myopic. So what has had happened between the often non-myopic great grandparents (and even earlier generations) and the grandparents of the present time? Something in the water?

3. Mothers' concerns: You must have heard mothers telling their children not to watch too much TV, play video games, surf the net, etc, or risk becoming near-sighted? So what is the truth - excessive near work precipitates myopization? If so, then reading/studying should be banned as well?

Speaking of myopization, what are the processes? Perhaps we can take some educated guesses:

Well, since high intraocular pressure is not associated with school myopia, we can probably rule out glaucoma genes. Of course, some argue that all myopes are glaucoma-suspects until proven otherwise. This is, however, a later complication, not a primary causative factor.

Structurally speaking, myopic eyes have very thin sclera and thin choroid as well. This seems to imply that (1) a re-arrangement of collagen fibers of the sclera, in other words, the thin sclera is not a result of ballooning from high intraocular pressure ; (2) a reduction of the blood volume in the choroid; and/or (3) an increase in vitreous cell production of vitreous collagen/hayluronic acid, i.e., an increase in the volume of the vitreous. A closer look into the biochemical mechanisms of all three then makes sense. Perhaps the starting point should be posterior staphyloma that usually is the chief culprit of exceedingly high myopia, e.g., -10D or more.

Posterior staphyloma is readily seen with either ultrasound B-scan or high-resolution orbital MRI. It is a small bulge out from the posterior pole. With A-scan, you'll be under the impression that the eye has long anterior-posterior axis. Current clinical studies of myopia progression are all based on A-scan which obviously cannot detect posterior staphyloma.

A quick note on the math of myopia: At roughly 1mm (along the anterior-posterior axis)=3D (diopter), you can see why myopia increases so quickly as 1D is equivalent to a mere 0.3mm, so an emmetropic eye is around 23mm "long", an eye with -10D refractive error will be 26.3mm "long" well tolerated within the orbit. Of course there must be an upper limit for the eye globe to fit into the orbit without the appearance of that in Graves Disease (i.e., exophthalmos). So an eye with -20D, or almost 28mm "long" will not move too freely when looking laterally. I have used long in quotes because this is a one-dimensional measurement. Myopic eyes are in fact huge in the 3-dimensional sense. Usually, an adult eyeball is 6.5ml and the orbit is 30ml in volume. Besides the eye, there are fat, blood vessels, the optic nerve, and the six extraocular muscles also. In Graves Disease, either the muscles or the orbital fats become bulky thereby forcing the eyeball outward.

Back to posterior staphyloma: Apparently some kind of signals have ordered an out-pouching of the posterior pole. Then we maybe looking at two different collagen fiber re-arrangements in the sclera, an early one for the school myopia and the later second for posterior staphyloma. And it should be a matter of identifying what these signals are. For example, growth factors or MMPs may have been dispatched in two waves by the emmetropization control center somewhere in the visual/cerebral cortex.

2 comments:

Anonymous
said...

Are there different types ofPosterior staphylomas? My son was born with one and I wanted to find out if it will be in his gene's now. We have no history of it in the family. He's had a strong contact since he was 5, he's 10. And has 20/40-20/40 in the eye. Could a posterior staphyloma be cause by birth trauma?

There are two types, type 1 involves the posterior pole and type 2, the macula. Neither is caused by birth trauma.

Posterior staphyloma can be from a congenital malformation resulting in high myopia. It is also seen in malignant myopia which, in some cases, is autosomal dominant (may involve loci at 18p11.31 and 12q21­23). The genes are most likely responsible for the development of posterior staphyloma.

In the absence of a family history and/or other systemic/ocular diseases, a congenital cause is more likely.